Among these modalities, inhibition of the renin-angiotensin-aldosterone system is generally considered the most important intervention.[7] The pathogenesis of CKD is complex, and existing studies suggest the involvement of the Wntβ-catenin signaling pathway, Transforming Growth Factor-β (TGFβ)-samds signaling pathway, Hippo/YAP signaling pathway, tumor necrosis factor (TNFα), HF-1, and P53.[9–11]. This evidence concerns the gene TP53 and chronic kidney disease.